Category Archives: All Updates

SMACC Gold Call for Abstracts

A reminder that the closing date for abstracts for the SMACC Gold conference is Friday 22nd November 2013.

Why should I care?

Remember this may well end up being the best critical care / emergency medicine / prehospital & retrieval medicine conference in the universe.
Submitting an abstract is good for you. As well contributing to education and the world medical knowledge base, you’ll get an extra line in the ‘academic’ section of your CV, which will make you at least appear smart.
What can you submit? This doesn’t have to be ground breaking research. Case reports, audits, topic reviews, and even ideas have been accepted as conference abstracts in the past (you’re building a picture of my CV now).
This means you still have time to come up with something, and submit it. What’s the worst thing that can happen? It’s like dating – as long as your self esteem can cope with rejection, you’re better off asking than not asking.
Submit here. You might get a yes, adding instant turgidity to your CV.
Remember also that it’s MUCH harder for your colleagues and/or employer to stop you going if you’re presenting a poster or oral session.

I have no financial interest in the SMACC Gold conference

Call-for-Abstracts-Flyer

Guidelines for the Management of Heart Failure

Some new guidelines to be aware of are the AHA Guidelines for the Management of Heart Failure. Full text is available free and while comprehensively covering chronic heart failure there is an interesting section on acute decompensated heart failure.
Evidence-based medicine enthusiasts might be interested in recommendations to consider dopamine, nesiritide, and ultrafiltration. These therapies also get a mention in the 2012 European Guidelines. I recommend you review the articles cited in the guidelines to make your own mind up.
Here are a couple of snippets you may find useful:


Snippet from American Guidelines: intravenous loop diuretic doses

“HF patients receiving loop diuretic therapy should receive an initial parenteral dose greater than or equal to their chronic oral daily dose; then dose should be serially adjusted.”


Snippet from European Guidelines: management algorithm for acute heart failure

Click to enlarge

AHF-ESC

2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary
Circulation. 2013 Oct 15;128(16):1810-52 Free Full Text
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012
Eur Heart J. 2012 Jul;33(14):1787-847 Free Full Text

Avoiding intubation in ARDS with awake ECMO

ECMOillusiconA letter in Intensive Care Medicine by Hoeper and colleagues from Hannover describes a small case series of six ARDS patients with severe hypoxaemia who went straight from non-invasive ventilation to awake veno-venous ECMO. All had single organ failure and four were immunocompromised, the latter factor influencing the decision to try to avoid invasive mechanical ventilation. Four of the six patients survived to hospital discharge. A larger multicentre study is being planned.

Clinical illustration courtesy of Dr Brian Burns

Extracorporeal membrane oxygenation instead of invasive mechanical ventilation in patients with acute respiratory distress syndrome
Intensive Care Med. 2013 Nov;39(11):2056-2057 (no abstract)

Even the dead exhale CO2

cadaverETCO2iconCardiac arrest patients sometimes have unrecognised oesophageal intubations because clinicians omit capnography, based on the assumption that circulatory arrest leads to an absence of exhaled CO2. This is wrong, and reassuringly the latest ILCOR cardiac arrest guidelines recommend waveform capnography during resuscitation.
Of interest is the fact that even corpses have CO2 in their lungs. While not clinically relevant, this may have value when fresh frozen cadavers are used for airway training, since we might be able to supplement the realism of airway instrumentation with the realism of connecting the capnography adaptor and circuit and seeing confirmation on the monitor.
This preliminary study, completed by my Sydney HEMS colleagues, needs further work, but it’s an interesting area.
Sustained life-like waveform capnography after human cadaveric tracheal intubation
Emerg Med J doi:10.1136/emermed-2013-203105
[EXPAND Abstract]


Introduction Fresh frozen cadavers are effective training models for airway management. We hypothesised that residual carbon dioxide (CO2) in cadaveric lung would be detectable using standard clinical monitoring systems, facilitating detection of tracheal tube placement and further enhancing the fidelity of clinical simulation using a cadaveric model.

Methods The tracheas of two fresh frozen unembalmed cadavers were intubated via direct laryngoscopy. Each tracheal tube was connected to a self-inflating bag and a sidestream CO2 detector. The capnograph display was observed and recorded in high-definition video. The cadavers were hand-ventilated with room air until the capnometer reached zero or the waveform approached baseline.

Results A clear capnographic waveform was produced in both cadavers on the first postintubation expiration, simulating the appearances found in the clinical setting. In cadaver one, a consistent capnographic waveform was produced lasting over 100 s. Maximal end-tidal CO2 was 8.5 kPa (65 mm Hg). In cadaver two, a consistent capnographic waveform was produced lasting over 50 s. Maximal end-tidal CO2 was 5.9 kPa (45 mm Hg).

Conclusions We believe this to be the first work to describe and quantify detectable end-tidal capnography in human cadavers. We have demonstrated that tracheal intubation of fresh frozen cadavers can be confirmed by life-like waveform capnography. This requires further validation in a larger sample size.

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How to Be a Hero

Kal-fly-iconI’m not a hero and don’t claim to be, but when I was given this talk to do for the SMACC 2013 conference I researched the topic and realised I’d worked with several of them.
The talk was the toughest I’ve ever given, because I cried while giving it, and knew that it wouldn’t just be the large audience in front of me who would know I was a wuss, but that it was being recorded for many others to find out too!

A full transcript of the talk, the slide set, and links to references from the talk can be found here.

Early surgery for intracerebral haemorrhage

ICHgraphicIconTo operate or not to operate on patients with an intracerebral haematoma? Deep ones can be tricky and risk damage to surrounding brain, so superficial ones may be more likely to benefit.
These patients with superficial lesions were assessed in STICH II, an international prospective randomised controlled trial comparing early surgery with conservative treatment.
Inclusion criteria were strict:

  • spontaneous lobar intracerebral haemorrhage on CT scan (≤1 cm from the cortical surface of the brain) with a volume of between 10 mL and 100 mL
  • within 48 h of onset
  • had a best motor score on the Glasgow Coma Score (GCS) of 5 or 6, and had a best eye score of 2 or more (ie, were conscious at randomisation).

The primary outcome was a Glasgow Outcome Scale-based evaluation of recovery (‘favourable’ vs ‘unfavourable’), which did not significantly differ between groups.
A predefined subgroup of patients with a poorer prognosis (using a score based on age, haematoma size and GCS) may have a better outcome with surgery. Some patients randomised to conservative therapy subsequently underwent delayed surgery. Thanks to appropriate intention-to-treat analysis they would have remained in the conservative treatment group which may have contributed to an underestimation of the benefit of surgery.
So, overall a negative trial, and patients with small lesions and higher GCS scores won’t benefit from surgery. Patients in poorer prognostic groups might benefit, but that remains unproven.
Some other ICH trials to be aware of are Clear III and MISTIE III, which are investigating thrombolytic agents in combination with clot removal, including with minimally invasive techniques.
Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial
Lancet. 2013 Aug 3;382(9890):397-408
[EXPAND Abstract]


BACKGROUND: The balance of risk and benefit from early neurosurgical intervention for conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intraventricular haemorrhage admitted within 48 h of ictus is unclear. We therefore tested the hypothesis that early surgery compared with initial conservative treatment could improve outcome in these patients.

METHODS: In this international, parallel-group trial undertaken in 78 centres in 27 countries, we compared early surgical haematoma evacuation within 12 h of randomisation plus medical treatment with initial medical treatment alone (later evacuation was allowed if judged necessary). An automatic telephone and internet-based randomisation service was used to assign patients to surgery and initial conservative treatment in a 1:1 ratio. The trial was not masked. The primary outcome was a prognosis-based dichotomised (favourable or unfavourable) outcome of the 8 point Extended Glasgow Outcome Scale (GOSE) obtained by questionnaires posted to patients at 6 months. Analysis was by intention to treat. This trial is registered, number ISRCTN22153967.

FINDINGS: 307 of 601 patients were randomly assigned to early surgery and 294 to initial conservative treatment; 298 and 291 were followed up at 6 months, respectively; and 297 and 286 were included in the analysis, respectively. 174 (59%) of 297 patients in the early surgery group had an unfavourable outcome versus 178 (62%) of 286 patients in the initial conservative treatment group (absolute difference 3·7% [95% CI -4·3 to 11·6], odds ratio 0·86 [0·62 to 1·20]; p=0·367).

INTERPRETATION: The STICH II results confirm that early surgery does not increase the rate of death or disability at 6 months and might have a small but clinically relevant survival advantage for patients with spontaneous superficial intracerebral haemorrhage without intraventricular haemorrhage.

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GOLDen Educational Opportunity!

smacc-gold-logo-2

 
SMACC was my all-time favourite conference ever. Its sequel, smaccGOLD, promises to be even better, as you’ll see from the program
The smaccGOLD online registration goes live this Monday 16th September at 8am in Sydney
This will be 11pm Sunday 15th in London, and 6pm Sunday 15th in New York
Make sure you don’t miss your chance to register for the best critical care conference ever!
Also check out the preconference workshops – a jawdropping line-up of medical masters covering everything you’d want to learn. The only difficult part is deciding what you won’t go to! Places are limited and expected will sell out quickly. Registration is on a first come basis.
Hopefully we’ll see you there.

smaccGOLD is a not-for-profit venture and I receive no payment for any participation in the conference or its promotion

Beta blockade in sepsis

tachy-iconWhat do septic patients need if they remain shocked after fluid resuscitation? Catecholamines right? Let’s stimulate some adrenoceptors and support that circulation!
Sydney’s Prof Myburgh has told us why adrenaline (epinephrine) and noradrenaline (norepinephrine) are the go-to vasoactive choices, and Prof Singer from London likes to remind us about the detrimental effects of these drugs – the pros and cons are listed here. Tachycardia is associated with worse outcomes in sepsis, and the balance of oxygen supply and demand can be difficult to achieve. Beta blocking drugs could reduce tachycardia, but there does seem to be something counter-intuitive about giving both beta-blockers and catecholamines in the same patient. You might expect that beta blockers would cause fall in cardiac output and worsen tissue perfusion.
A small study previously showed possible helpful effects of beta blockers in children with burns. The potential benefits may extend beyond control of heart rate to anti-inflammatory / anti-catabolic effects. A recent publication evaluated beta blockers in adult patients with septic shock, which appears to be a pilot study for an ongoing randomised controlled trial.
They included patients who had been fluid resuscitated and who required noradrenaline, and treated them with a titrated esmolol infusion commenced at 25 mg/hr, with an upper dose limit of 2,000 mg/hr, to maintain a predefined HR range between 80 and 94 beats per minute. Esmolol was chosen because of its half-life of approximately 2 min, so any adverse effects could be rapidly reversed. They examined the macrocirculation using pulmonary artery catheterisation and the microcirculation using sublingual microvascular blood flow imaging.
Most of the patients had pneumonia, and interestingly, all patients received intravenous hydrocortisone (200mg/d) as a continuous infusion.
In this small cohort of patients, they found that titrating the heart rate to less than 95 bpm was associated with maintenance of stroke volume and preservation of microvascular blood flow. Although cardiac output fell because of the lower HR, stroke volume, MAP, and lactate levels were unchanged while noradrenaline requirements were reduced.

Increased vascular reactivity to norepinephrine following nonselective β-blockade is supported by volunteer and animal studies, and postulated mechanisms include:

  • blockade of a peripheral β2-mediated vasodilatory effect of noradrenaline
  • decreased clearance of infused noradrenaline
  • a centrally mediated effect on reflex activity
  • inhibition of vascular endothelial nitric oxide synthase activity

Microvascular Effects of Heart Rate Control With Esmolol in Patients With Septic Shock: A Pilot Study
Crit Care Med. 2013 Sep;41(9):2162-2168
[EXPAND Abstract]

 

OBJECTIVE: β-blocker therapy may control heart rate and attenuate the deleterious effects of β-stimulating catecholamines in septic shock. However, their negative chronotropy and inotropy may potentially lead to an inappropriately low cardiac output, with a subsequent compromise of microvascular blood flow. The purpose of the present pilot study was to investigate the effects of reducing heart rate to less than 95 beats per minute in patients with septic shock using the β-1 adrenoceptor blocker, esmolol, with specific focus on systemic hemodynamics and the microcirculation.

DESIGN: Prospective, observational clinical study.

SETTING: Multidisciplinary ICU at a university hospital.

MEASUREMENTS AND MAIN RESULTS: After 24 hours of initial hemodynamic optimization, 25 septic shock patients with a heart rate greater than or equal to 95 beats per minute and requiring norepinephrine to maintain mean arterial pressure greater than or equal to 65 mm Hg received a titrated esmolol infusion to maintain heart rate less than 95 beats per minute. Sublingual microcirculatory blood flow was assessed by sidestream dark-field imaging. All measurements, including data from right heart catheterization and norepinephrine requirements, were obtained at baseline and 24 hours after esmolol administration. Heart rates targeted between 80 and 94 beats per minute were achieved in all patients. Whereas cardiac index decreased (4.0 [3.5; 5.3] vs 3.1 [2.6; 3.9] L/min/m; p < 0.001), stroke volume remained unchanged (34 [37; 47] vs 40 [31; 46] mL/beat/m; p = 0.32). Microcirculatory blood flow in small vessels increased (2.8 [2.6; 3.0] vs 3.0 [3.0; 3.0]; p = 0.002), while the heterogeneity index decreased (median 0.06 [interquartile range 0; 0.21] vs 0 [0; 0]; p = 0.002). PaO2 and pH increased while PaCO2 decreased (all p < 0.05). Of note, norepinephrine requirements were significantly reduced by selective β-1 blocker therapy (0.53 [0.29; 0.96] vs 0.41 [0.22; 0.79] µg/kg/min; p = 0.03).

CONCLUSIONS: This pilot study demonstrated that heart rate control by a titrated esmolol infusion in septic shock patients was associated with maintenance of stroke volume, preserved microvascular blood flow, and a reduction in norepinephrine requirements.

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Xenon – no bull?

Xenon, an inert ‘noble’ gas with proven anaesthetic properties, has possible neuroprotective properties and appears to be also cardioprotective in this small study of post-cardiac arrest patients. Its high viscosity affects airway resistance, resulting in higher peak pressures and the need for a strategy to avoid gas trapping (ie. longer expiratory times as with asthma). Apparently it’s expensive, but these results suggest further study is warranted.
Feasibility and Cardiac Safety of Inhaled Xenon in Combination With Therapeutic Hypothermia Following Out-of-Hospital Cardiac Arrest
Crit Care Med. 2013 Sep;41(9):2116-24
[EXPAND Abstract]


OBJECTIVES: Preclinical studies reveal the neuroprotective properties of xenon, especially when combined with hypothermia. The purpose of this study was to investigate the feasibility and cardiac safety of inhaled xenon treatment combined with therapeutic hypothermia in out-of-hospital cardiac arrest patients.

DESIGN: An open controlled and randomized single-centre clinical drug trial (clinicaltrials.gov NCT00879892).

SETTING: A multipurpose ICU in university hospital.

PATIENTS: Thirty-six adult out-of-hospital cardiac arrest patients (18-80 years old) with ventricular fibrillation or pulseless ventricular tachycardia as initial cardiac rhythm.

INTERVENTIONS: Patients were randomly assigned to receive either mild therapeutic hypothermia treatment with target temperature of 33°C (mild therapeutic hypothermia group, n = 18) alone or in combination with xenon by inhalation, to achieve a target concentration of at least 40% (Xenon + mild therapeutic hypothermia group, n = 18) for 24 hours. Thirty-three patients were evaluable (mild therapeutic hypothermia group, n = 17; Xenon + mild therapeutic hypothermia group, n = 16).

MEASUREMENTS AND MAIN RESULTS: Patients were treated and monitored according to the Utstein protocol. The release of troponin-T was determined at arrival to hospital and at 24, 48, and 72 hours after out-of-hospital cardiac arrest. The median end-tidal xenon concentration was 47% and duration of the xenon inhalation was 25.5 hours. The frequency of serious adverse events, including inhospital mortality, status epilepticus, and acute kidney injury, was similar in both groups and there were no unexpected serious adverse reactions to xenon during hospital stay. In addition, xenon did not induce significant conduction, repolarization, or rhythm abnormalities. Median dose of norepinephrine during hypothermia was lower in xenon-treated patients (mild therapeutic hypothermia group = 5.30 mg vs Xenon + mild therapeutic hypothermia group = 2.95 mg, p = 0.06). Heart rate was significantly lower in Xenon + mild therapeutic hypothermia patients during hypothermia (p = 0.04). Postarrival incremental change in troponin-T at 72 hours was significantly less in the Xenon + mild therapeutic hypothermia group (p = 0.04).

CONCLUSIONS: Xenon treatment in combination with hypothermia is feasible and has favorable cardiac features in survivors of out-of-hospital cardiac arrest.

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Lowering the BP rapidly in ICH

ICH-iconIn our retrieval service case reviews, one thing that is that sure to generate discussion is what to do about the blood pressure in patients who present with intracranial haemorrhage and hypertension. We don’t want the bleeding to be worsened by higher blood pressure, but we don’t want to decrease cerebral perfusion pressure in patients who have raised intracranial pressure. Consensus guidelines exist for spontaneous intracerebral haemorrhage and subarachnoid haemorrhage, but they’re not based on strong data.
Here’s a study that attempted to provide more information. Intensive lowering to a target systolic of 140 mmHg within 1 hour was compared with lowering to a target of 180 mmHg. There was no significant reduction in the rate of the primary outcome of death or severe disability. The skeptic in me is disappointed there was no placebo arm. An ordinal analysis of modified Rankin scores favoured the intensive BP-lowering intervention, which means this study can be used by both those for and against intensive BP lowering to support their views.
As explained in an accompanying editorial, a number of factors may limit generalisability to Western practice, such as the predominant use of the alpha-blocking agent urapadil in the large numbers of Asian patients, a drug not available in the United States. Future publication of the ATACH-II trial using intravenous nicardipine will shed more light on this topic.
1. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage
N Engl J Med. 2013 Jun 20;368(25):2355-65
[EXPAND Abstract]


BACKGROUND: Whether rapid lowering of elevated blood pressure would improve the outcome in patients with intracerebral hemorrhage is not known.

METHODS: We randomly assigned 2839 patients who had had a spontaneous intracerebral hemorrhage within the previous 6 hours and who had elevated systolic blood pressure to receive intensive treatment to lower their blood pressure (with a target systolic level of <140 mm Hg within 1 hour) or guideline-recommended treatment (with a target systolic level of <180 mm Hg) with the use of agents of the physician’s choosing. The primary outcome was death or major disability, which was defined as a score of 3 to 6 on the modified Rankin scale (in which a score of 0 indicates no symptoms, a score of 5 indicates severe disability, and a score of 6 indicates death) at 90 days. A prespecified ordinal analysis of the modified Rankin score was also performed. The rate of serious adverse events was compared between the two groups.

RESULTS: Among the 2794 participants for whom the primary outcome could be determined, 719 of 1382 participants (52.0%) receiving intensive treatment, as compared with 785 of 1412 (55.6%) receiving guideline-recommended treatment, had a primary outcome event (odds ratio with intensive treatment, 0.87; 95% confidence interval [CI], 0.75 to 1.01; P=0.06). The ordinal analysis showed significantly lower modified Rankin scores with intensive treatment (odds ratio for greater disability, 0.87; 95% CI, 0.77 to 1.00; P=0.04). Mortality was 11.9% in the group receiving intensive treatment and 12.0% in the group receiving guideline-recommended treatment. Nonfatal serious adverse events occurred in 23.3% and 23.6% of the patients in the two groups, respectively.

CONCLUSIONS: In patients with intracerebral hemorrhage, intensive lowering of blood pressure did not result in a significant reduction in the rate of the primary outcome of death or severe disability. An ordinal analysis of modified Rankin scores indicated improved functional outcomes with intensive lowering of blood pressure.

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2. Blood pressure in intracerebral hemorrhage–how low should we go?
N Engl J Med. 2013 Jun 20;368(25):2426-7